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OB13Obstetrics Toronto Notes 2023

Medications

• most drugs crossthe placenta to some extent

• very few drugs are teratogenic, but very few drugs have proven safety in pregnancy

• use any drug with caution and only if necessary

• analgesics:acetaminophen preferable to ASA or ibuprofen

Table 7. Documented Adverse Effects, Weigh Benefits vs. Risks, and Consider Medication

Change

Contraindicated Medication Adverse Effect

ACE Inhibitor

Carbamaztpine

Chloramphenicol

lithium

Misoprostol

NSAIDs

Phcnytoin

Fetal renal defects, IUGR,oligohydramnios

ONTO in1-2%

Grey baby syndrome (fetal circulatory collapse 2’to toxic accumulation)

Ebstein's cardiac anomaly, goitre, hyponatremia

Mobius syndrome (congenital facial paralysis with or without limb delects),spontaneous abortion.P1l

Premature closure ol theductusarteriosus after 30 wk Gt (prior to that, indomelhacin used for tocolysis)

Fetal hydantoin syndrome in 5-10% (IUGR.mental retardation,facial dysmorphogenesis.congenital

anomalies)

CNS,craniofacial,cardiac,and thymic anomalies

Anti folate properties,therefore theoretical risk in T1; risk of kernicterusin T3

Stainsinfant'

steeth, mayaffect long bone development

Congenital malformation (including ONTO) up to9%

Increased incidence of spontaneous abortion,stillbirth, prematurity, IUGR.fetal warfarin syndrome (nasal

hypoplasia, epiphysealstippling, oplic atrophy, mental retardation, intracranial hemorrhage)

Drug Resources During Pregnancy and

Breastfeeding

• Hale T. Medications and mothers'

milk, 18th ed. Springer Publishing

Company, 2019

• Lactmed: https://toxnet.nlm.nih.gov/

nowtoxnet/lactmed.htm

Retinoids(e.g.Accutane'

)

Sulpha drugs

Tetracycline

Valproate

Warfarin

Immunizations

Intrapartum

• administration is dependent on the risk of infection vs. risk of immunization complications

• safe:tetanus toxoid, diphtheria, influenza, hepatitis B, and pertussis

• avoid live vaccines (risk of placental and fetal infection):polio, measles/mumps/rubella, and varicella

• contraindicated: oral typhoid

• the Public Health Agency of Canada recommends:

all pregnant women receive the influenza vaccine

all pregnant women should be given Tdap every pregnancy irrespective of immunization history.

Ideally between 27-32 wk GA but can be given at 13-26 wk GA if high-risk of PTL

Postpartum

• rubella vaccine for all non-immune mothers. If they have had an adult booster and remain nonimmune, they should not be revaccinated and pregnancy should be deferred for at least 1 mo following

vaccination

• hepatitis B vaccine should be given to infants within 12 h of birth if maternal status unknown or

positive or if father is known to have chronic hepatitis B infection -follow-up doses at I and 6 mo

• any vaccine required/recommended is generally safe postpartum

• delayed postpartum vaccination is recommended if patient receives immunoglobulin or blood

products(e.g. Rhlg or packed red blood cells)

Radiation

• ionizing radiation exposure is considered teratogenic at high doses

if indicated for maternal health,should be done

• imaging not involving direct abdominal/pelvic high dosage radiation is not associated with adverse

effects

• higher dosage of radiation to fetus occurs with plain x-ray of lumbarspine/abdomen/pelvis,

barium enema,CT abdomen/pelvis/lumbar spine

• radioactive isotopes of iodine are contraindicated

• no known adverse effects from U/S or MKI (long-term effects of gadolinium unknown, avoid if

possible)

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OBM Obstetrics Toronto Notes 2023

Table 8. Approximate Fetal Doses from Common Diagnostic Procedures

Examination Estimated Fetal Dose (cGy) Number of Exams Safe in Pregnancy

Plain Film

Abdomen

Pelvis

Lumbar spine

Thoracicspine

Cbest|2 views)

014 35

0-11 45

0-17 29 Radiation in Pregnancy

• Necessary amount to cause

miscarriage:>5 cGy

• Necessary amount to cause

malformations:>20-30 cGy

0.009 555

<0.001 5000

Cl

Abdomen 0-8 e

Pelvis

Lumbar spine

Chest

2-5 2

0-24 20

0.006 833

Adapted from:Cohen-Kefem.et al.2005 and Valentin 2000

Antepartum Hemorrhage

•see Gynaecology, First and Second Trimester Bleeding, GY20

Definition

•vaginal bleeding from 20 wk GA to term

Differential Diagnosis

•bloody show (represents cervical changes/early stages of dilation) - most common physiologic

etiology in T3

•placenta previa

•placental abruption - most common pathological etiology in T3

•vasa previa

•cervical lesion (cervicitis, polyp, ectropion, cervical cancer)

•uterine rupture

•other: bleeding from bowel or bladder, abnormal coagulation

Table 9. Comparison of Placenta Previa and Abruptio Placentae

Placenta Previa Abruptio Placentae

Definition Abnotmal location of the placenta neat, partially, or

completely over the internal cervical os

Idiopathic

0.5 0.8% of all pregnancies

History of placenta previa |4-8% recurrence risk)

Multiparity

Increased maternal age

Multiple gestation

Uterine tumour (e.g. fibroids) or other uterine

anomalies

Uterine scar due to previous abortion, CO. D&C.

myomectomy

Premature separation of a normally implanted placenta

after 20 wk GA

Etiology

Epidemiology

Risk Factors

Idiopathic

1-2% of all pregnancies

Previous abruption (recurrence rate 5-16%)

Maternal HIN (chronic or gestational HTN in 50% of

abruptions) or vascular disease

Cigarette smoking (>1pack/d), excessive alcohol

consumption, cocaine

Multiparity and/or maternal age >35 yr

PPR0M

Rapid decompression of a distended uterus

(polyhydramnios, multiple gestation)

Uterine anomaly, fibroids

Trauma (e.g. motor vehicle collision,maternal battery)

Bleeding PAINLESS Usually PAINFUL

Placenta Previa

Definition

• placenta implanted in the lowersegment of the uterus covering the internal cervical os (either fully or

partially)

• placental location is described in relation to the internal os as “mm away" or “mm of overlap"

Clinical Features

• PAINLESS bright red vagina) bleeding (recurrent), may be minimal and cease spontaneously but can

become catastrophic

• mean onset of bleeding is 30 wk GA, but onset depends on degree of previa

• physical exam

• do not perform digital vaginal exam until ruled out placenta previa (speculum and transvaginal

probe are safe)

• uterus soft and non-tender

• presenting fetal part high or displaced

• i

'

HR usually normal

shock /anemia correspond to degree of apparent blood loss

Do NOT perform a vaginal exam until

placenta previa has been ruled out

byU/S

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0B15Obstetrics Toronto Xotes 2023

•complications

• fetal

• perinatal mortality low but still higher than with a normal pregnancy

• prematurity (bleeding often dictates early CD)

• intrauterine hypoxia (acute or 1UGR)

• fetal malpresentation

» PPROM

• risk of fetal blood lossfrom placenta, especially if incised duringCD

• maternal

• <1% maternal mortality

• hemorrhage and hypovolemic shock, anemia, acute renal failure,and pituitary'necrosis

(Sheehan syndrome)

• placenta accreta -especially if previous uterine surgery or anterior placenta previa

• hysterectomy

Investigations

•transvagina] U/Sis more accurate than transabdominal U/S at diagnosing placenta previa at any GA

•spontaneously resolution islikely with increasing uterine distention if the placenta covers the internal

os by <20 mm at 20 wk GA

•transvaginal U/S should be repeated in T3as continued change in the placental location islikely

Management

•goal:keep pregnancy intrauterine until the risk of continuing pregnancy outweighs the risk of

preterm delivery

•stabilize and monitor

• maternal stabilization:large bore IV with hydration, O’

for hypotensive patients

maternal monitoring: vitals, urine output, blood loss, blood work (hematocrit,CBC,1NR/PTT,

fibrinogen, FDP,type,and crossmatch)

• EFM

• U/Sassessment:when fetal and maternal conditions permit, determine fetal viability, GA, and

placentallocation

•Rhogam* if motheris Rh-negative

•Plow Cytometry'and Kleihauer-Betke methods determine extent of fetomaternal transfusion and this

helpsto administer Rhogam* at adequate dose

•<37 wk GA and minimal bleeding:expectant management

• admit to hospital

• limited physical activity, no douches, enemas,orsexual intercourse

consider corticosteroidsfor fetal lung maturity

delivery when fetusis mature or hemorrhage indicating maternal or fetal compromise

. >37 wk GA:deliver by CD

Placental Abruption

Definition

• partial or total placental detachment that is premature and caused by bleeding at the decidual *

placental interface

• occurs >20 wk GA (placental detachment <20 wk GA is classified as an abortion)

Clinical Features

• classification

total (fetal death inevitable) vs.partial

external/revealed/apparent:blood dissects downward toward cervix

internal/concealed/occult (20%):blood dissects upward toward fetus,may or may not present

with vaginal bleeding

most are mixed

Placental abruption is the most common

cause of DICin pregnancy

• presentation

usually PAINFUL (80%) vaginal bleeding (bleeding not always present if abruption is concealed),

uterine tenderness, uterine contractions/hypertonus(lack of relaxation between contractions)

pain:sudden onset, constant,localized to lower back and uterus

• shock/anemia out of proportion to apparent blood loss

± fetal distress,fetal demise (15% present with demise), bloody amniotic fluid (fetal presentation

typically normal)

± coagulopathy

Complications

• fetal complications: perinatal mortality 25-60%, prematurity, intrauterine hypoxia

• maternal complications: <1% maternal mortality, disseminated intravascular coagulation (DIG)

(in 20% of abruptions), acute renal failure, anemia, hemorrhagic shock,pituitary necrosis (Sheehan

syndrome),amniotic fluid embolus

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0616Obstetrics Toronto Notes 2023

Investigations

• clinicJdiagnosis, U/S not sensitive for diagnosing abruption (sensitivity 15%)

Management

• maternal stabilization: large bore IV with volume replacement,O’for hypotensive patients

• maternal monitoring: vitals, urine output, blood loss, blood work (hematocrit, CBC, PTT/PT,

fibrinogen, FDP, type, and crossmatch)

. EFM

• blood products on hand (red cells, platelets, cryoprecipitate) because of DIC risk

• Rhogam* if Rh negative

How Cytometry and Kleihauer-Betke test to assess dosing of Rhogam*, may confirm abruption

(notdiagnostic)

• abruption without fetal/maternal compromise (mild abruption)

<37 wk GA: use serial hematocrit to assess concealed bleeding,deliver when fetus is mature or

when hemorrhage dictates

>37 wk GA:stabilize and deliver

• abruption with fetal/maternal compromise (moderate to severe abruption)

• hydrate and restore blood loss and correct coagulation defect if present

vaginal delivery if no contraindication and no evidence of fetal or maternal distress

« CD iflive fetus and fetal or maternal distress develops with fluid/blood replacement, labour fails

to progress, or if vaginal delivery otherwise contraindicated

Kleihauer-Betke Test

Quantifiesfetal cells in the maternal

circulation

Vasa Previa

Definition

• unprotected fetal vessels pass over the cervical os; associated with velamentous insertion of cord into

membranes of placenta or succenturiate (accessory) lobe

Epidemiology

• I in 5000 deliveries - higher in twin pregnancies

Clinical Features

• PAINLESS vaginal bleeding and fetal distress (tachy-to-bradyarrhvthmia in a sinusoidal pattern)

• ifundiagnosed, 50% perinatal mortality, increasing to 75% if membranes rupture (most infants die of

exsanguination)

• ifdiagnosed antenatally on U/S without labour or symptoms,then 97% survival

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Figure 3.Vasa previa Investigations

• Apt test ( NaOH mixed with the blood) can be done immediately to determine if the source of bleeding

is fetal (supernatant turns pink) or maternal (supernatant turns yellow)

• Wright’

sstain on blood smear and look for nucleated red blood cells(in cord, not maternal blood)

Management

planned CD (35-36 wk GA) or ifbleeding, emergency CD (since bleeding is from fetus, a small amount

ofblood loss can have catastrophic consequences)

Obstetrical Complications

Preterm Labour

Definition

• labour between 20 and 37 wk GA

PTL isthe most common cause of

neonatal mortality in the United Sates

and is within the top 5causes of

Etiology neonatal mortality in Canada

• idiopathic

• maternal: infection (recurrent pyelonephritis, untreated bacteriuria, chorioamnionitis), HTN, DM,

chronic illness, mechanical factors(previous obstetric, gynaecological, and abdominal surgeries);

socio-environmental (poor nutrition,smoking, drugs, alcohol, stress), preeclampsia, advanced

reproductive age

• maternal-fetal: PPROM, polyhydramnios,placenta previa, placental abruption, placental insufficiency

• fetal:multiple gestation, congenital abnormalities, fetal hydrops

• uterine:excessive enlargement (hydramnios,multiple gestation), malformations (intracavitary

leiomyomas,septate uterus,and Mullerian duct abnormalities)

Positivefetal fibronectin in

cervicovaginal fluid (>50 ng/mL) at 24

wk GA predicted spontaneous PTL at <34

wk GA with sensitivity 23%,specificity

97%,PPV 25%, NPV 96%

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Epidemiology +

• PTL complicates about 10% of pregnancies

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OB17 Obstetrics Toronto Notes 2023

Risk Factors

• prior history of spontaneous PTL is the most important risk factor

• prior history of large or multiple cervical excisions (cone biopsy) or mechanical dilatation (D&C)

• cervical length: measured by transvaginal U/S (cervical length >30 mm has high negative predictive

value for PTL before 34 wk GA)

• identification of bacterial vaginosis and Vrcaplasma ureatyticum infections

• routine screening not supported by current data, but it is reasonable to screen high-risk women

• family history of preterm birth

• smoking

• late maternal age

• multiple gestation

• cocaine

Ultrasooographic Cervical length Assessment in

RietfKiiwg Preterm Birth in Singleton Pregnancies

J Ohstet EfaetnlCan 2018:40:154-161

ieeoaaendations:

tIrjrsajdo~ra ultrasonography should not he

atifor cenrkal length assessnre nt to predict

preterm beta (II-2D)

2Tranvagral eltrasooograplty is the preferred

ralefor cervical assessment to identify worn en

at f creased risk of spoirtan eo us preterm b irth

end may he offeredlo non at mcreased risk of

preterm bets(11-28)

llraapenreel uSrasooographj may be offered

to aomeo at increased risk of preterm birth

Itransvaipa!uitasKiography iseither

unacceptable or cneratahle (11-28)

4.3ecaase of poor postve p redictive values

Edsenstilies and lack of proven effective

.nteneiDoss,rouine transvaginal cervical lenglb

assessmea is not recommended in women at

lenv-nsk (ll-2{)

5k wocnec presecing wits suspected PH.

iansvagaa sonograph.

-c assessment of cervical

engtb may he used to help m determining who isat

kgb-rsk of preterm delivery and may be helpful in

preveaag unnecessary intervention. It is unclear

whether Bismformaion resultsin a reduced risk of

pteara birth (H-2B)

6.kr asymptomat icwomen with a history

of spontaneous preterm birth and an

ultrasonograsbicalfy diagnosed short cemcal

engtb («25om) pror a 24 wk GA.cervical cerda ge

shogfd he ctmsdered to reduce the risk of preterm

KAMI

J.hr al asymptomaic women who present with

membranes at or protruding past the external

cervical os.a:emergency cerclage should be

cresiered a reduce the risk of pieterm delivery

Prevention of Preterm Labour

A. Cervical Cerclage

• definition:placement of cervicalsutures at the level of the internal os, usually at the end ofT1 or in T2

and removed in T3

• indications:cervical incompetence (i.e.cervical dilation and effacement in the absence of increased

uterine contractility)

• diagnosis of cervical incompetence

• obstetrical Hx:silent cervical dilation, recurrent T2 losses, cervical proceduressuch as loop

excisions

ability of cervix to hold an inflated Foley catheter during a hysterosonogram

• transvaginal U/S of cervical length is recommended only for high-risk pregnancies and only

before 28 wk GA

• proven benefit in the prevention of PTL in women with primary structural abnormality of the cervix

(e.g. conization of the cervix, connective tissue disorders)

B. Progesterone

• progesterone thought to maintain uterine quiescence; however, exact mechanism of action is unclear

• indicated if cervical length is <25 mm at <24 wk GA

• if short cervix:200 mg vaginally once daily from time of diagnosis to 36 wk GA

• if risk factors or Hx of PTL present,give vaginally starting at 16-20 wk GA

• superior to cerclage in preventing PTL ofsingletons not due to cervical incompetence

C.Lifestyle Modification

• smoking cessation,substance use reduction, treatment of GU infections (including asymptomatic

UT'

Is), and patient education regarding risk factors

'Hf

Predicting Preterm Labour

• fetal fibronectin:a qlvcoprotein in amniotic fluid and placental tissue

positive if >50 ng/mL;SPV > PPV

• done if one or more signs of PTL (regular contractions >6/h, pelvic pressure, low abdominal pain

and/or cramps, low backache)

• done only if: 24-34 wk GA, intact membranes, <3 cm dilated, established fetal well-being

contraindicated if:cerclage, active vaginal bleeding, vaginal exam, or sex in last 24 h

• if negative, not likely to deliver in 7-14 d (>95% accuracy); if positive, increased risk of delivery,

may need admission/transfer to centre that can do delivery ± tocolysis and/or corticosteroids

Physical Examination -Indicated Cerclage:A

Systematic Review and Meta-Analysis

(hat Gynecol 2017:126:125-135

Pirpose Jo estimate the effectiveness of physical

eBBinabon-micaad cerclage ct the setting ol 12

cemcal dilatation

Methods:VeB-analyss of studies identified on

MEDUliE.EM8A5E.Scopus.CliricalTnals.gov.Web of

Scenes.EdteCoctrane Library

Results "

0txia s.757 women|485 underwent

cerdageEd 272 were expectantly managed).Studies

extpered cerdage with oo cerclage in women with a

physics: exam naior Bat revealed cervical dilatation

of >0.5 cm between 14 an d 27wk GA.Survival was

core kkely ia tecerclage group (71ft) compared to

Be expectant:,-e-aged grojp (47%) (RR-1.65, 95%

Q L19-2T!|.Cerclage was dso associated with a

sign scan:pro ongat or of pregnancy (average 33.98

d.95% Q17.88-50.081. greater GA at delivery (mean

dfference462 wk.95% Cl 3.89-5.361and significant

•>1.Dees m preterm birtt between 24 and 28 wk GA

(newpared to 37%:8R-0.23.95% 00.13-0.41|

sd at lessthan 34 wk GA (50% com pared to 82%;

RM.SS.95% Cl 0.38-0.80)

Conclusions P-yskalexanir.a;ion-indicated

cerdage is associated with sgnScaut reductions

e peraatal mortality and pietetm birtti.RCTsare

warranted for additional investigation

Clinical Features

• regular contractions(2 in 10 min, >6/h)

• cervix >1 cm dilated, >80% effaced, or length <2.5 cm

Management

A. Initial

• transfer to appropriate facility ifstable

tocolysis and first dose of antenatalsteroids prior to transfer

• hydration (normalsaline at 150 mL/h)

• bed rest in LLDP to reduce aortocaval compression and improve cardiac output

• analgesia (morphine)

• avoid repeated pelvic exams (increased infection risk)

• U/S examination of fetus(GA, BPP,presentation, placenta location, EFW)

• prophylactic antibiotics (for GBS); important to consider if PPROM (e.g. erythromycin controversial,

but may help to delay delivery)

B.Tocolysis (Suppression of Labour)

• does not inhibit PT L completely, but may delay delivery (used for <48 h) to allow for betamethasone

valerate (Celestone* ) and/or transfer to appropriate centre for care of the premature infant

• requirements (all must be satisfied):

• PTL

• live, immature fetus,intact membranes, cervical dilatation of <4 cm

• absence of maternal or fetal contraindications

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OBIS Obstetrics Toronto Notes 2023

• contraindications:

• maternal:bleeding (placenta previa or abruption), maternal disease (HTN, DM, heart disease),

preeclampsia or eclampsia, chorioamnionitis

• fetal:erythroblastosis fetalis,severe congenital anomalies, fetal distress/demise, lUCiR, multiple

gestation (relative)

Tocolylicjfor Preterm Prenuturt Rupture o <

Membranes

C otluane OBSyst ter 20I4:2:CD007062

Purpose: To assess the potential Ite.

-eSts ard hatms

of tocolysis in women with PPROM

Selection Criteria: Pregnant women with srg'eto:

pregnancies and PPROM (23-36-6 wkGA)

Results:8 studies with 498 women tota .

Prophylactic tocolysiswith PPROM was associated

with increased overall latency,w.thoot additional

banelits for maternal/neonatal outco-ies.Foe

women with PPROM hefore 34 wk GA.there was a

significantly increased risk of chorioamnomtis in

women who received tocolysis.Neonatal outcomes

t significantly different

Conclusions Although there are Imitationstolhf

studies, there Is currently muffiotnt evidence to

supporttotolyk therapy lot women with PPROM. at

there was an increase In maternal ehonoamiiiMitij

withoutsignificant benefits to the infant

• agents:

calcium channel blockers: nifedipine

20 mg PO loading dose followed by 20 mg PO 90 min later

20 mg can be continued q3-8 h for 72 h or to a maximum of 180 mg

10 mg PO q20 min x 4 doses

relative contraindications: nifedipine allergy, hypotension, hepatic dysfunction, concurrent

p-mimetics or MgSOq use, transdermal nitrates, or other antihypertensive medications

absolute contraindications: maternal CHF, aortic stenosis

• prostaglandin synthesis inhibitors: indomethacin

• first-line for early PTL (<32 wk GA) or polyhydramnios

• 50-100 mg PR loading dose followed by 25-50 mg q6 h x 8 doses for 48 h

• contraindications: renal/hepatic impairment, peptic ulcer disease

G. Antenatal Corticosteroids

•betamethasone valerate (Celestone*) 12 mg IM q24 h x 2 doses or dexamethasone 6 mg 1M ql 2 h x 4

doses

• given between 24 to 34+6 wk GA if expected to deliver in the next 7 d

• patients between 22+0 and 23+6 wk GA at high-risk of preterm birth within the next 7 d should

be provided with multidisciplinary consultation regarding high likelihood for severe perinatal

morbidity and mortality and associated maternal morbidity - consider antenatal corticosteroid

therapy if early intensive care is requested and planned

specific maternal contraindications:active I B

•enhance fetal lung maturity, reduce perinatal death, and reduce incidence of severe RDS, 1VH,

necrotizing enterocolitis, or neonatal sepsis

D. Neuroprotection

•MgSO t 4 g bolus followed by 1 g/h infusion for at least 4 h if imminent delivery expected and 533+ 6

wk GA

Ml . II ' j

Prematurity increases newborn risk of:

• Respiratory distress

• Hypoglycemia

• Hyperbilirubinemia

• Apnea

• Feeding difficulties

• Seizures

• And more

Prognosis

• prematurity is the leading cause of perinatal morbidity and mortality

•24 wk GA = 50% survival ( may be higher in tertiary care centres with level 3-4 NICU)

•30 wk GA or 1500 g (3.3 lb)

= 90% survival

•33 wk GA or 2000 g (4.4 lb)

= 99% survival

•morbidity due to asphyxia, hypoxia, sepsis, RDS, IV H, thermal instability, retinopathy of prematurity,

bronchopulmonary dysplasia, necrotizing enterocolitis

Prelabour Rupture of Membranes

Definitions $

• PROM: prelabour rupture of membranes

• prolonged ROM:>18 h elapsed between ROM and onset of labour

. PPROM: preterm (hefore 37 wkGA) AND PROM

Membrane status determined by

• Pooling of fluid on speculum exam

• Increased pH of vaginal fluid

(nitrazine test)

• Ferning of fluid under light

microscopy Risk • Decreased AFV on U5

Factors

• maternal: multiparity, cervical incompetence, infection (cervicitis, vaginitis, STI, UT1), family history

of PROM, low socioeconomic class/poor nutrition

• fetal: congenital anomaly, multiple gestation

• other risk factors associated with PTL Antibiotic Therapy in Preterm FurnitureRupture

ol the Membranes

J 0 bstet Gynaecol Can 2017:39:207 212

Recommendations:

1.Fo!lowing PPROM. antibiobesshould be

administered towomen who are notin labour

in ntdei to prolong pregnancy and to decrease

maternal and neonatal morbidity

2.The benefit of antibioticsisgreater at earlier GAs

3.Art b Dtics of choice are penitillins or macrotide

antibiotics (erythromycin} in parenteral ardor oral

forms.In patients aiergic to penicillin,macro'

de

antibioticsshould be used alone

4. Ivin possible regimen optionsfiom large PPROM

RCfsare:|1|ampcillin 2 g IVq6 h and erythromycin

260 mg IV qG h for 48 h followed by amoi < bn 250

mg PO q8 h ard erythromycin 333 mg PO qS h lot 5

d:(2) erythromycin 260 mg PO qG b for 10 d

5.Amoucillm/clavulanic acid should not be used

be cause of an uicicased risk ol necrotizing

enlerocolibsln neonates.Amoilcillm without

davutanlc add Issafe

{.Women presenfmg with PPROM should be screened

for Oils.SIls.and CBS

Clinical Features

• history of fluid gush or continued leakage

Investigations

• sterile speculum exam (avoid introduction of infection)

pooling of fluid in the posterior fornix

cascading:fluid leaking out of cervix with cough/valsalva

• nitrazine (basic amniotic fluid turns nitrazine paper blue)

low specificity as it can also be positive with blood, urine, or semen

• ferning:salt in amniotic fluid evaporates, giving amniotic fluid the appearance of ferns on microscopy

• U/S to rule out fetal anomalies (if no prior routine anatomy scan ); assess El'W, presentation, and BPP

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OB19 Obstetrics Toronto Notes 2023

Management

• admit for expectant management and monitor vitals q4 h, daily NST, WBC count,surveillance for

infection

• avoid introducing infection by minimizing vaginal examinations

consider administration of betamethasone valerate (Celestone*) to accelerate maturity if <35 wlc

GA and no evidence of infection

consider tocolysis for 48 h to permit administration of steroidsif PPROM induceslabour

• screen patients for UTTs, STIs, GBS infection, and treat with appropriate antibiotics if positive (treat

GBSattime of labour)

• if not in labour or labour not indicated, consider antibiotics: penicillins or macrolide antibiotics are

the antibiotics of choice

• deliver urgently if evidence of fetal distress and/or chorioamnionitls

Table 10. PROM Management

Gestational Age Management

22-25 wk Individual consideration with counselling of parentsregarding risks to

preterm infants

Expectant management as prematurity complications aresignificant

“Grey zone"where risk of death from RDS and neonatalsepsisisthe

same

26-34 wk

34-36 wk

>37wk Induction of laboursince (he risk of death from sepsisis greater than

IDS

Prognosis

• varies with GA

• 90% of patients with PROM at 28-34 wk GA go into spontaneous labour within I wk

• 50% of patients with PROM at <26 wk GA go into spontaneous labour within I wk

• complications: cord prolapse, intrauterine infection (chorioamnionitis), premature delivery, limb

contracture, and pulmonary hypoplasia especially if PROM occurs at very early GA

Postterm Pregnancy

Definition

• pregnancy >42 wk GA

Epidemiology

• 41 wk GA: up to 27%

• >42 wk GA: 5.5%

Etiology

• most cases are idiopathic

• anencephalic fetus with no pituitary gland

• placental sulfatase deficiency (X-linked recessive condition, incidence ranges from 1 in 2000 to 1 in

6000 births)

• incorrect dates

Management (for singleton, cephalic fetus, otherwise uncomplicated)

• labour induction is recommended at 41+3 wk GA if no contraindications to vaginal delivery (see

Induction and Augmentation of Labour, OB3S)

Prognosis

• if >42 wk GA, perinatal mortality 2-3x higher (due to progressive uteroplacental insufficiency)

• with increasing GA, higher rates of: intrauterine infection, asphyxia, meconium aspiration syndrome,

placental insufficiency, placental ageing and infarction, macrosomia, dystocia,fetal distress, operative

deliveries, pneumonia,seizures, NICU admission,stillbirth

• morbidity increased with gestational HTN,DM, placental abruption,1UGR, advanced reproductive

age, and multiple gestation

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Intrauterine Fetal Demise s

Definition

• fetal demise in utero after 20 wk GA (before 20 wk GA is called spontaneous abortion)

Epidemiology

• occurring in 1% of pregnancies, increased in high-risk pregnancies

Etiology

• 50% idiopathic

• 50% secondary to HTN,DM, erythroblastosis fetalis, congenital anomalies,umbilical cord or

placental complications,intrauterine infection, and APS

Clinical Features

• decreased perception of FM by mother

• SFH and maternal weight not increasing

• absent fetal heart tones on Doppler (not diagnostic)

• high MSAFP

• on U/S:no FHR.Depending on timing of death, may see skull collapse,brain tissue retraction, empty

fetal bladder, non-filled aorta, or poor visualization of midline falx

DIC:Generalized Coagulation and Fibrinolysis

Leading lo Depletion ol Coagulation Factors

Obstetrical Causes

•Placental abruption

•Gestational HTN

•Fetal demise

PPH

DIC-specific Blood Wort

•CBC (platelets)

•aPIT and PT [prothrombin time)

•TOP

Fibrinogen

Treatment

• Treat underlying cause

• Supportive

• Fluids

• Blood products

• FFP, platelets, cryoprecipitate

• Consider anti-coagulation as tfTEpropbplaiis

Management

• diagnosis:absent cardiac activity and FM on U/S (required)

• determine secondary cause

maternal:HbAk,fasting glucose, TSH, Kleihauer-Betke, VDRL, ANA,CBC,anticardiolipins,

antibody screens,1NR/PTT,serum/urine toxicology screens,cerv ical and vaginal cultures, and

TORCH screen

• fetal:karyotype, cord blood,skin biopsy, genetics evaluation, autopsy, amniotic fluid culture for

CMV, parvovirus B19,and herpes

placenta:pathology,bacterial cultures

Treatment

• >20 wk GA:10L with vaginal misoprostol (Cytotec*)

• monitor for maternal coagulopathy (10% risk of DIC)

• parental psychological care/bereavement support as per hospital protocol

• comprehensive discussion within 3mo about final investigation and post-mortem results,help make

plansfor future pregnancies

Intrauterine Growth Restriction

Definition

• failure of a fetusto reach its biologically determined growth potential due to pathological factors

Etiology/Risk Factors

• 50% unknown

• maternal:

malnutrition,smoking, drug misuse, alcoholism, cyanotic heart disease,T1DM,SLE, pulmonary

insufficiency', previous 1UGR (25% risk), chronic HTN,gestational HTN,chronic renal

insufficiency',prolonged gestation TORCH

To xoplasmosis

Others:e.g. syphilis

Rubella

CMV

• placental:

any disease that causes placental insufficiency

• gross placental morphological abnormalities (infarction, hemangiomas,placenta previa, and

abnormal cord insertion)

HSV

• fetal: See Table 15.0B31

TORCH infections, multiple gestation, and congenital anomalies/chromosomal abnormalities

(10%)

Clinical Features

• symmetric/type1(25-30%);occurs early in pregnancy

reduced growth of both head and abdomen

• HC/AC ratio may be normal (>1 up to 32 wk GA;

=1 at 32-34 wk GA; <1 after 34 wk GA)

• usually associated with congenital anomalies or TORCH infections

• asymmetric/type 11 (70%):occurslate in pregnancy

fetal abdomen is disproportionately smaller than fetal head

• brain isspared; therefore HC/AC ratio increased

usually associated with placental insufficiency

more favourable prognosis than type I

• complications

prone to meconium aspiration, asphyxia, polycythemia, hypoglycemia, hypocalcemia,

hypophosphatemia,hyponatremia, and intellectual disability

greater risk of perinatal morbidity and mortality

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0B21 Obstetrics Toronto Notes 2023

Investigations

•SFH measurements at ever)'antepartum visit (ensure accurate GA)

•if mother at high-risk or SFH lags >2 cm behind GA

• U/S for biparietal diameter, HC/AC ratio, FL,fetal weight, AFV (decrease associated with 1UGR),

and decrease in the rate of growth

. ± BFP

• Doppler analysis of umbilical cord blood flow

Management

•prevention via risk modification prior to pregnancy is ideal

•modify controllable factors:smoking, alcohol, nutrition,and treat maternal illness

•serial BPP (monitorfetal growth) and determine cause of 1UGR,if possible

•deliver)'when extrauterine existence isless dangerous than continued intrauterine existence

(abnormal function tests, absent grow'th,severe oligohydramnios) especially if >34 wk GA

•optimize fetus with betamethasone valerate (telestone*), MgSO 4 for neuroprotection, early GBS swab,

and paediatrics consult if anticipated preterm delivery

• as 1UGR fetuses are lesslikely to withstand stresses of labour, they are more likely to be delivered by

CD

Macrosomia

Definition

• infant weight S90th percentile for a particular GA or >4000 g

Etiology/Risk Factors

- maternal obesity,gestational and pre-gestational DM, past history of macrosomic infant,prolonged

gestation, multiparity,excessive maternal weight gain during pregnane)'

Clinical Features

• increased risk of perinatal mortality

• CPD and birth injuries(shoulder dystocia,fetal bone fracture) more common

• complications of DM in labour (see Table 14,OB30)

Investigations

• serial SFH

• U/S for EFW if mother at high-risk or SFH >2 cm ahead of GA

Management

• prevent hyperglycemia in patients with DM, optimize pre-pregnancy weight, and limit excessive

pregnancy weight gain in patients with increased BM1

• planned CD is a reasonable option where EFW >5000 g in non-diabetic patients and EFW >4500 g in

diabetic patients

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AL GRAWANY

OB22 Obstetrics Toronto Notes 2023

Polyhydramnios/Oligohydramnios

Table 11. Polyhydramnios and Oligohydramnios

Polyhydramnios Oligohydramnios

Definition AFI >25 cm

U/S:single deepest pocket >8 cm

AM «S cm

U S: single deepest pocket s2 cm

Etiology Idiopathic most common

Maternal

I10M:abnormalities of transchorionic flow

Idiopathic most common

Maternal

Uteroplacental insufficiency (preeclampsia,

nephropathy)

Medications (ACEI)

Maternal-fetal

Chonoangiomas

Multiple gestation

Fetal hydrops (increased erythroblastosis)

Fetal

Congenital urinary tract anomalies (renalagenesis,

obstruction,posterior urethral uahres)

Demise/chronic hypoiemia (blood shunt away from

kidneys to perfuse brain)

Fetal

Chromosomal anomaly (up to 2/3 of fetuses

have severepolyhydramnios)

Respiratory: cystic adenomatoid malformed IUGR

Ruptured membranes:prolonged amniobc fluid leak

Amniotic fluidnormally decreases after 35 wk CA

lung

CNS:anencephaly.hydrocephalus,

meningocele

fit:tracheoesophageal fistula,duodenal

atresia,facial clefts (interfere with

swallowing)

Epidemiology Occurs in 0.2-1.6% of allpregnancies Occurs in -4.SNof allpregnancies

Severe form in"

0.7%

Common in pregnancies>4t wk £A (

'

12c)

Uterus smal for dates

Fetal complications

15-25 c have fetal anomalies

Amniotic fluidbands (11) can lead toPotter's facies,

limb deformities,abdominal wall defects

Obstetrical complications

Cord compression

Increasedrisk of adverse fetal outcomes

Pulmonary hypoplasia (late-oosel)

Marker for infants who may not toleratelabour well

Always warrants admission and investigation

Rule outROM

fetalmonitoring IBS!.BPP)

U S Doppler studies (umb lical cord andutenne

artery)

Maternalhydration with oral or IV fluids to help

increase amniotic fluid

Injection of fluid via amniocentesis will improve

condition for «1wk - may be most helpful for

visualizing any associated fetal anomalies

Consider delivery if term

Ammo-infusion may be considered during labour na

intrauterine catheter

Poorer withearly onset

High mortality related to congenita!malformations

and pulmonary hypoplasia when diagnosedduring 12

Clinical Features and Complications Uterus large for GA.difficulty palpating fetal

parts and hearing FHR

Maternal complications

Pressure symptoms from overdistended

uterus (dyspnea,edema,hydronephrosis)

Obstetrical complications

Cord prolapse,placental abruption,

malpresentation.P1L.uterine dysfunction.

andPPH

Determine underlying cause

Screen for maternal disease/infection

Complete fetal U/S evaluation

Depends on severity

Mild to moderate cases require no treatment

If severe,hospitalize and consider

therapeutic amniocentesis

Management

Prognosis 2- to 5-foldincrease inrisk of perinatal

mortality

Antenatal Depression

Definition

• major depression occurring in a patient who is pregnant, onset may be prior to pregnancy

Epidemiology

• occurs in 7-9% of pregnancies

Risk Factors

• prior history of depression, anxiety, unintended or unwanted pregnancy, life stress, intimate partner

violence or history of abuse, poor social support, chronic general medical conditions (specifically

hypothyroidism)

Clinical Features

• comparable to symptoms of non-pregnant major depressive disorder (see Psvchiatrv. PS12)

• suspect if: prior history of depression, excessive anxiety about the fetus, poor self-esteem,

despondency, anhedonia, non-adherence to antenatal care, poor weight gain due to decreased appetite

or inadequate diet,suicidal ideation

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OB23 Obstetrics Toronto Notes 2023

Assessment

• Edinburgh Postnatal Depression Scale or others

Treatment

• antidepressants, psychotherapy,supportive care, and electroconvulsive therapy if refractory or if

features of psychosis, catatonia,high risk ofsuicide, and fluid or food refusal leading to dehydration

and malnutrition

Prognosis

• may be associated with altered fetal physiologic effects, adverse pregnancy and neonatal outcomes,

abnormal infant and child development, or cognitive impairment and psychopathology in the

offspring, leading to lasting long-term effects

• increased risk of recurrence after pregnancy, and conversion of the diagnosis to bipolar disorder

Multi-Fetal Gestation and Malpresentation m

Epidemiology

• incidence of twins is 1 in 80 and triplets is 1 in 6400 in North America

• 2/3 of twins are dizygotic (fraternal)

risk factors for dizygotic twins:1V E, increased maternal age, newly discontinued OCP, and

ethnicity (e.g.certain African regions)

• monozygous twinning occurs at a constant rate worldwide (1 in 250)

• determine zygosity by number of placentas, thickness of membranes,sex, and blood type

Clinical Features

The

m

Ps of Multiple Gestation

Complications

Increased rates of:

Puking

Pallor (anemia)

Preedampsia/Pregnancy-induced HTN

Pressure (compressive symptoms)

PTL. PROM ' PPROM

Polyhydramnios

Placenta previa/abruption

PPHlAntepartum hemorrhage

Prolonged labour

Cord Prolapse

Prematurity

Malpresentation

Perinatal morbidity and mortality

Parental distress

Postpartum depression

Table 12. Complications Associated with Multiple Gestation

Maternal Uteroplacental Fetal

Increased PROM PTL

Polyhydramnios

Placenta previa

Placental abrupbon

Increased physiologicalstress on allsystems PPH (uterine atony)

Increased compressive symptoms Umbilical cord prolapse

Hyperemesis gravidarum Prematurity

IUGB

Malpresentation

Congenital anomalies

Twin-twin transfusion syndrome

Increased perinatal morbidity and mortality

Twin interlocking (twin A breech,twin S vertex)

Single fetal demise

GDM

Gestational HTN

Anemia

CO Cord anomalies

Thrombosis (velamentousinsertion.2 vessel cord)

Management

• U/S determination of chorionicity must be done within T1 (ideally 8-12 wk GA)

• increased antenatalsurveillance

• serial U/S q2-3 wk from 16 wk GA (monochorionic),q3-4 wk from 18-22 wk GA (uncomplicated

diamniotic dichorionic) to assess growth

Doppler flow studies weekly if discordant fetal growth (>30%)

• BPP

• may attempt vaginal delivery (if dichorionic diamniotic or monochorionic diamniotic) if twin A

presents as vertex and growth discrepancy <25%, otherwiseCD (40-50% of all twin deliveries, 10% of

cases have twin A delivered vaginally and twin B delivered by CD)

• all monochorionic monoamniotic twins need to be delivered by CD

• mode of delivery depends on fetal weights,GA, chorionicity, and presentation of presenting twin

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OB24 Obstetrics Toronto Xotes 2023

Monoamniotic Monoamniutic Monoamniotic

Monochorionic Monochorionic Monochorionic

(forked cord) *9-12 d (one cord)

Diamniotic Diamniotic Diammotic

Dichorionic Dichorionic Monochorionic

(fused) *0 *4-8 d -72 h (separated)

Figure 4. Classification of twin pregnancies

•Indicates time of cleavage

Twin-Twin Transfusion Syndrome

Definition

• formation of placental intertwin vascular anastomoses that can cause arterial blood from donor twin

to passinto veins of the recipient twin

Epidemiology

• 10% of monochorionic twins

• concern if >30% discordance in EFW

Clinical Features

• donor twin:IUGR, hypovolemia, hypotension, anemia, and oligohydramnios

• recipient twin:hypervolemia, HTN, CH1

;

, polycythemia, edema, polyhydramnios, and kernicterus in

neonatal period

Investigations

• detected by U/S screening, Doppler flow analysis

Management

• fetoscopic laser ablation of placental vascular anastomoses (preferred between 16-26 wk GA)

• therapeutic serial amniocentesisto decompress polyhydramnios of recipient twin and decrease

pressure in cavity and on placenta

• intrauterine blood transfusion to donor twin if necessary

Breech Presentation

Definition

• fetal buttocks or lower extremity is the presenting part as determined on U/S

Criteria for Vaginal Breech Delivery

• Frank or complete breech. >36 wk GA

. EFW 2500-3800 g based on clinical

and U/S assessment15.5-8.5lb)

• Fetal head flexed

• Continuous fetal monitoring

• Two experienced obstetricians,

assistant, and anesthetist present

• Ability to perform emergency CD

within 30 min if required

• Mother motivated for vaginal breech

delivery and understandsrisks and

benefits

• complete (10%): hips and knees both flexed

• frank (60%): hips flexed, knees extended, buttocks present at cervix

• most common type of breech presentation

most common breech presentation to be delivered vaginally

• incomplete (30%):both or one hip partially flexed and both or one knee present below the buttocks,

feet or knees present first (footling breech, kneeling breech)

Epidemiology

• occurs in 3-4% of pregnancies at term (25% at <28 wk GA) +

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OB25Obstetrics Toronto Notes 2023

Risk Factors

• maternal: pelvis (contracted), uterus(shape abnormalities,fibroids, previous breech), pelvic tumours

causing compression, and grand multiparity

• placental: placenta previa

• fetal: prematurity, amniotic fluid (poly-/oligohydramnios), multiple gestation, congenital

malformations (found in 6% of breeches; 2-3% if in vertex presentations), abnormalities in fetal tone

and movement, aneuploidy, hydrocephalus, and anencephaly

Management

• pre- or early-labour U/S to assess type of breech presentation, fetal growth, estimated weight, placenta

position, attitude of fetal head (flexed is preferable); if U/S unavailable, recommend Cl)

• KCV and elective CD should be presented as options with the risks and benefits outlined; obtain

informed consent

• ECV: procedure that is performed with external pressure on the uterus to encourage a non-vertex

fetus (breech, transverse, or oblique) to turn into vertex presentation

overallsuccess rate of -40-60%

criteria:>36 wk GA,singleton, unengaged presenting part, reactive NST, intact membrane

contraindications:

absolute:where CD is required (placenta previa, previous classical CD), previous

myomectomy, PROM, uteroplacental insufficiency, non-reactive NST,multiple gestation

relative: mild/moderate oligohydramnios,suspected 1UGR, HTN, previous T3 bleed, nuchal

cord

risks: abruption, cord compression, cord accident, ROM,labour,fetal bradycardia requiring CD

(<1% risk), alloimmunization,fetal death (1/5000)

method: tocometry,followed by U/S guided transabdominal manipulation of fetus with constant

FHR

if patient Rh negative, give Rhogam' after the procedure

better prognosis if multiparous, good fluid volume,small baby,skilled obstetrician, and posterior

placenta

if unsuccessful, planned vaginal breech birth or planned CD

• vaginal breech delivery: can be spontaneous or assisted

method:

encourage effective maternal pushing efforts

at delivery of aftercoming head, assistant must apply suprapubic pressure to flex and engage

fetal head

delivery can be spontaneous or assisted; avoid fetal traction

apply fetal manipulation only after spontaneous delivery to level of umbilicus

contraindications: cord presentation, footling breech, fetal factors incompatible with vaginal

delivery (e.g. hydrocephalus, macrosomia,1UGR),clinically inadequate maternal pelvis

• CD recommended if: the breech has not descended to the perineum in the second stage of labour after

2 h,in the absence of active pushing,or if vaginal delivery is not imminent after 1 h of active pushing

Prognosis

• regardless of route of delivery,breech infants have lower birth weights and higher rates of perinatal

mortality,congenital anomalies, abruption, and cord prolapse

A.Complete Breech

B. Frank Breech

C. Incomplete Breech ®

Figure 5.Types of breech

presentation

Hypertensive Disorders of Pregnancy

Hypertension in Pregnancy

•hypertensive disorders of pregnancy arc classified as either pre-existing or tie novo (gestational HTN

or preeclampsia) and exist on a spectrum Ominous Symptoms of HTN in

Pregnancy

Right upper quadrant pain

Headache

Visual disturbances

PRE-EXISTING HYPERTENSION

Definition

•sBP 140 mmHg or dBP S90 mmHg p

15 min apart on the same arm,seated with appropriate sized cuff

•essential HTN is associated with an increased risk of gestational HTN, abruptio placentae, 1UGR, and

1U1-D

rior to 20 wk GA; BP should be elevated on S2 occasions at least

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GESTATIONAL HYPERTENSION

Definition

•sBP >140 mmHg or dBP >90 mmHg after 20 wk GA without proteinuria in a patient known to be

normotensive before pregnancy +

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OB26 Obstetrics Toronto Xotes 2023

PREECLAMPSIA

Definition

• pre-existing or gestational HTN with new onset proteinuria ( urinary protein:creatinine ratio >30 mg/

mmol) or adverse conditions(end organ dysfunction)

ECLAMPSIA

Definition

• the occurrence of >1 generalized convulsion and/or coma in the setting of preeclampsia and in the

absence of other neurologic conditions

Etiology

• placental malperfusion -» soluble factors released into circulation -> maternal vascular endothelial

injury -> hypertension + multi-organ injury

Epidemiology of Eclampsia

• an eclamptic seizure occurs in approximately 0.5% of mildly preeclamptic patients and 2-3% of

severely preeclamptic patients

Clinical Manifestation of Eclampsia

• eclampsia is a clinical diagnosis

• typically tonic-clonic and lasting 60-75 s

• symptoms that may occur before the seizure include persistent frontal or occipital headache, blurred

vision, photophobia, right upper quadrant or epigastric pain, and altered mentalstatus

• in up to one third of cases, there is no proteinuria or hypertension prior to the seizure

• approx 25% of cases will present in the postpartum period

• in general, women with typical eclamptic seizures who do not have focal neurologic deficits or

prolonged coma do not require diagnostic evaluation, including imaging

Risk Factorsfor Hypertensive Disorders in Pregnancy

• maternal factors:

primigravida (80-90% of gestational HTN), first conception with a new partner,PMHx or FMHx

of gestational HTN,or preeclampsia/eclampsia

• DM, chronic HTN,or renal insufficiency

obesity'

APS or inherited thrombophilia

extremes of maternal age (<18 or >35 yr)

• previousstillbirth or1UFD

vascular or connective tissue disease

• fetal factors:

lUGRorolieohvdramnios

• GTN

multiple gestation

• fetal hydrops'

mirrorsyndrome"

abruptio placentae

Clinical Evaluation of Hypertensive Disorders in Pregnancy

• in general, clinical evaluation should include the mother and fetus

• evaluation of mother

• body weight

• central nervoussystem

presence and severity of headache

visual disturbances (blurring,scotomata)

tremulousness,irritability’, and somnolence

hyperreflexia

hematologic (bleeding, petechiae)

hepatic (right upper quadrant or epigastric pain,severe N/V)

• renal (urine output, colour)

• evaluation of fetus:

FM

FHR tracing - NST

• U/S for growth

BPP

• Doppler flow studies

Laboratory Evaluation of Hypertensive Disorders in Pregnancy

• CBC

• PIT, INR, fibrinogen -if abnormal LFT'

s or bleeding

• ALT, AST

• creatinine, uric acid

• 24 h urine collection for protein or albumin:creatinine ratio

• may consider placental growth factor (P1GF) testing orsFlt-1:P1GF ratio as an early screening test for

suspected preeclampsia

Eclampsia prior to 20 wk 6A is rare

and should raise the possibility of an

underlying molar pregnancy or APS

Hypertension in Pregnancy

Adverse Maternal Conditions

• sBP >160 mmHg

• dBP'

-100 mmHg

• HELIP

• Cerebral hemorrhage

• Renal dysfunction: oliguria <500

ml/d

• left ventricular failure, pulmonary

edema

• Placental abruption. DIC

• Abdominal pain. N/V

• Headaches,visual problems

• SOB.chest pain

• Eclampsia: convulsions

Adverse Fetal Conditions

• IUGR

• Oligohydramnios

• Absent/reversed umbilical artery end

diastolic flow

, Can result in fetal disability and

-

1

or death

Evidence

©- Recommendation Highlights of S06C

Clinical Practice Guidelines

Dag nosis, Evaluation, and Management of the

Hypertensive Disorders of Pregnancy

J Dbslet Gynaecol Can 2022.44:517 521

•low-risk nnrmolensive women shouldnat he

screened for proteinuria

•Home automated BP monitoring shoaldhensedto

mitigate wlrite-coatsyndrome

•Ca t jr -

.- . . . •

is recommended for women with low dietary intake

of calcium (<900 mg,'d)

• :

;

:r fie;: a -;s = : i.f :

risk women,low-dose ISA|S1or 162 rag'd) is

recomme nd ed f rom irefore 16 wk GA nnti 36 ok 61

•Exercise is recommended a prevent preeclampsia

•Antihypertensive therapy is recommended for

all pregnant women with sflP >140 marHg ordBP

>90 mmHg

•Initial anti-hypertensive therapy forsevere hTI

(sBf >160 mmHg or dBP >110 nnHg|sho _!d ne wrr

labetalol, nifedipine, methyidopa.orrydraaire

•Initial antihypertensive therapy for non-serere

HTN|BP 140-159/90-109 mmH$shoe: jie wnh

labetolol, nifedipine,or methyldopa

•Antenatal carticosteroidsfor feta, ring

maturation should oe cors dered ‘

ora l women

with proeclampsia Before 34 wk 6A 1« women

with pie eclampsia, initiation ol dehrery is

recommended at 37 wk GA

•MgSOi is the recommended fcst-lae treafeatfir

eclampsia and eclampsia prophylaxis in the case of

severe preeclampsia +

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OB27 Obstetrics Toronto Notes 2023

Complications of Hypertensive Disorders in Pregnancy

• maternal

liver and renal dysfunction

seizure - “eclampsia”

abruptio placentae

• left ventricular failure/pulmonary edema

D1C (release of placental thromboplastin consumptive coagulopathy)

HELLP syndrome

hemorrhagic stroke (50% of deaths)

• fetal (secondary to placental insufficiency)

• IUGR, prematurity, abruptio placentae, 1UED

Management of Hypertension

• for non-severe HTN (BP 149-159/90-109 mmHg): target a BP of 130-155/80-105 mmHg in patient

without comorbidities or <140/90 mmHg in patient with comorbidities

antihypertensive therapy for both pre-existing and gestational HTN: labetalol 100-400 mg PO

BID-T1D, nifedipine XL preparation 20-60 mg PO once daily or BID, or a-methyldopa 250-500 mg

PO BID-TID

• for severe HTN (BP>160/110 mmHg): target sBP <160 mmHg and dBP <110 mmHg, give one of:

• labetalol 20 mg IV,then 20-80 mg IV q30 min (max 300 mg), then switch to oral

nifedipine immediate release 5-10 mg capsule q30 min

• hydralazine 5 mg IV, repeat 5-10 mg IV q30 min or 0.5-10 rng/h IV, to a maximum of 20 mg IV (or

30 mg IM)

• no AGiI , AKBs, diuretics (may be used in cases of pulmonary edema or cardiac failure), prazosin, or

atenolol

• pre-existing HTN and gestational HTN without any deterioration

then decide to induce shortly thereafter

HELLP Syndrome

Hemolysis

Elevated

Liver Enzymes

Low

Platelets

can be followed until 37 wk GA,

Management of Preeclampsia

• if stable and no adverse conditions (24-33-16 wk GA): expectant management ± delivery as

approaching 34-36 wk GA(must weigh risks of fetal prematurity vs. risks of developing

preeclampsia/eclampsia)

antenatal corticosteroidsshould be considered if 35 wk GA

• if >37 wk GA, delivery is recommended

• for severe preeclampsia,stabilize and deliver, regardless of GA

• if severe preeclampsia during labour, increase maternal monitoring: hourly input and output, hourly

neurological vitals, and continuous l-

'

HR monitoring

• antihypertensive therapy (regimen as above forsevere H TN )

• seizure prevention:

MgSO t:4 g IV loading dose,followed by lg/h

postpartum management

risk of seizure highest in first 24 h postpartum - continue MgSO*

for 12-24 h after delivery

vitals ql h

• consider HELLP syndrome

most return to a normotensive BP within 2 wk

severe

Management of Eclampsia

. ABCs

• roll patient into LLDP to prevent aspiration

• supplemental O’

via face mask to treat hypoxemia due to hypoventilation during convulsive episode

• aggressive antihypertensive therapy for sustained sBP >160 mmHg or dBP >109 mmHg or with

hydralazine or labetalol

• prevention of recurrent convulsions:to prevent the possible complications of repeated seizure activity

(e.g.rhabdomyolysis, metabolic acidosis, aspiration pneumonitis, etc.)

• MgSO*

is the first-line therapy for eclampsia (used for treatment and prophylaxis)

• the definitive treatment of eclampsia is DELIVERY after maternal stabilization, irrespective of GA

or fetal distress, to reduce the risk of maternal morbidity and mortality from complications of the

disease

mode of delivery is dependent on the clinical situation and fetal-maternal condition

Differential Diagnosis of Cause for

Seizure in a Pregnant Woman

. Stroke

. Hypertensive disease

(hypertensive encephalopathy,

pheochromocytoma)

• Space-occupying lesion of the CNS

• Metabolic disorders (hypoglycemia.

SIADH)

• Infection (meningitis, encephalitis)

• TTP or thrombophilia

• Idiopathic epilepsy

• Use of illicit drugs

• Cerebral vasculitis

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